Rapid alterations in glucose transport and metabolism have been shown in rat adipocytes after fasting and refeeding. The mechanism for this was examined in rats fasted for 48 h and sacrificed plus and minus 6d of refeeding. Adipocytes from fasted rats show a 67% decrease in insulin-stimulated glucose transport activity compared to nonfasted control rats and a corresponding decrease in glucose transporters in the plasma membranes. Fasting is associated with fewer glucose transporters in the basal low-density microsomes and a diminished translocation of glucose transporters from the low-density microsomes to the plasma membranes with insulin. Adipocytes from the refed rats show a 49% overshoot in insulin-stimulated glucose transport activity compared to the control rats with only a l3% increase in glucose transporters in the plasma membranes. The concentration of basal low-density microsomal glucose transporters appears lower in the refed rats compared to the control rats but total intracellular glucose transporters were increased due to a 53% increase in low-density microsomal protein. These results suggest that insulin resistance at the glucose transport level induced by fasting is due to a depletion of intracellular glucose transporters. In contrast, the hyperresponsive insulin-stimulated glucose transport activity associated with refeeding is not totally accounted for by a change in the number of glucose transporters and may also involve modulation of glucose transporter intrinsic activity.